Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary function and exercise tolerance were measured before and after three saturation dives to a pressure of 3.7 MPa. The atmospheres were heliox with partial pressures of oxygen of 40 kPa during the bottom phase and 50 kPa during the compression and decompression phase. The bottom times were 3, 10, and 13 days. Decompression time was 13 days. Precordial Doppler monitoring was done daily during the decompression, and an estimate of the total bubble load on the pulmonary circulation was calculated as the accumulated sum of bubble scores recorded for each diver. Nine of the 18 divers had chest symptoms with retrosternal discomfort or nonproductive cough after the dive. There were no changes in dynamic lung volumes. Transfer factor for carbon monoxide was significantly reduced from 12.3 +/- 1.2 to 10.9 +/- 1.3 mmol.kPa-1.min-1 (P less than 0.01), and maximum oxygen uptake was reduced from 3.98 +/- 0.36 to 3.42 +/- 0.37 l/min STPD (P less than 0.01) after the dives. Resting heart rate was increased from 64 +/- 6 to 75 +/- 8 min-1 (P less than 0.01). The ventilatory requirements in relation to oxygen uptake and carbon dioxide elimination were significantly increased (P less than 0.01) after the dives. The physiological dead space fraction of tidal volume was significantly higher and showed an increase with larger tidal volumes (P less than 0.05). Anaerobic threshold estimated from gas exchange data decreased from an oxygen uptake of 2.30 +/- 0.25 to 1.95 +/- 0.28 l/min STPD (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise tolerance and pulmonary gas exchange after deep saturation dives. 236 82

Prostacyclin (PGI2) is one of several prostanoids released after antigen challenge of human lung fragments. To define its activity on human airways, we studied the effect of inhaled PGI2 in 10 normal and 8 asthmatic subjects. In random order, PGI2, 1 mg/ml, its hydrolysis product, 6-oxo-PGF1 alpha, 1 mg/ml, and glycine vehicle were given on separate occasions by nebulizer. Measurements of specific airway conductance (SGaw), blood pressure (BP), heart rate (HR), plasma 6-oxo-PGF1 alpha, and cyclic AMP levels were made at frequent intervals for as long as 45 min after nebulization. Prostacyclin and 6-oxo-PGF1 alpha caused cough and retrosternal discomfort. None of the drugs had any significant effect on SGaw in either the normal or asthmatic subjects, though 2 asthmatics showed consistent bronchodilatation with prostacyclin. Prostacyclin caused a marked fall in diastolic blood pressure (mean 20 +/- 3 mmHg) and increase in heart rate (29 +/- 3 beats X min-1) with a small late fall in systolic blood pressure (8 +/- 2 mmHg). This was associated with a 12- to 15-fold increase in plasma 6-oxo-PGF1 alpha levels maximal at 1 min, and in normal subjects only, a later twofold increase in plasma levels of cyclic AMP maximal at 5 min. Thus, inhaled PGI2 at concentrations that had pronounced cardiovascular activity produced no consistent effect on airway caliber in normal or asthmatic subjects.
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PMID:Airway and cardiovascular responses to inhaled prostacyclin in normal and asthmatic subjects. 298 91

The effect of inhaled capsaicin, the irritant extract of pepper, on airway tone has been studied in humans. Inhaled capsaicin (2.4 X 10(-10) and 2.4 X 10(-9) mol) caused a dose-dependent fall in specific airways conductance (maximum fall 28 +/- 19 and 38 +/- 19%, respectively; means +/- SD, n = 17). This was maximal within 20 s of exposure and lasted for less than 60 s. There was no difference in the magnitude or duration of bronchoconstriction between normal, smoking, or asthmatic subjects. Capsaicin also caused coughing and retrosternal discomfort. On repeated exposure to capsaicin, there was no evidence for a reduced response (tachyphylaxis). Ipratropium bromide (0.25 mg by inhalation) significantly (P less than 0.05) reduced the bronchoconstriction (maximum falls 34 +/- 14 and 15 +/- 9% after saline and ipratropium bromide, respectively; means +/- SD n = 6), indicating that it was dependent on a cholinergic vagal reflex rather than on local release of substance P from nerves in the airway. Inhaled sodium cromoglycate (10 mg by nebulizer or 40 mg as a dry powder), however, had no significant effect on the bronchoconstrictor response. Capsaicin may be a useful tool for investigating nonmyelinated nerve reflexes in human airways.
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PMID:Bronchoconstrictor response to inhaled capsaicin in humans. 315 68

The effect of bradykinin was studied by inhalation in normal and asthmatic human subjects, as well as on human bronchial smooth muscle in vitro. Bradykinin caused cough and retrosternal discomfort in all subjects and bronchoconstriction in asthmatic subjects. Bradykinin was approximately 10 times more potent than histamine and methacholine, and there was a significant correlation between the subjects' sensitivity to histamine and bradykinin. Bradykinin-induced bronchoconstriction was prolonged when compared with that of histamine and the C-fiber stimulant capsaicin. This bronchoconstriction was subject to tachyphylaxis, which was also associated with desensitization of the subjects to inhaled histamine. The provocative dose causing a 35% fall in specific airway conductance (PD35) was unaffected by aspirin (1 g orally). However, ipratropium bromide (0.25 mg by nebulizer) significantly inhibited the effect of bradykinin, the PD35 being 0.8 mumol (range, 0.16 to 3.4) and 0.15 mumol (range, 0.047 to 1.15) after active dose and placebo, respectively (p less than 0.05). Likewise, cromolyn sodium (40 mg dry powder) also significantly reduced response to bradykinin, with a PD35 of 0.04 mumol (range, 0.13 to 0.31) after placebo and 0.39 mumol (range, 0.05 to 4.45) after SCG (p less than 0.05). Bradykinin only weakly constricted human bronchial smooth muscle in vitro. Bradykinin at 10(-4) caused only 21.5 +/- 5.5% of the maximal carbamylcholine contraction in 11 of 18 airways. Captopril did not enhance the effect of bradykinin. Bradykinin is a potent bronchoconstrictor of human airways in vivo, acting in part through cholinergic mechanisms but not because of the formation of prostaglandins.
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PMID:Bradykinin-induced bronchoconstriction in humans. Mode of action. 354 15

The term adult respiratory distress syndrome (ARDS) was first introduced by Ashbaugh and Petty more than two decades ago. Since then, our understanding of this clinicopathologic entity has increased significantly. However, little therapeutic progress has been achieved, and the mortality remains high. ARDS is characterized by diffuse pulmonary microvascular injury resulting in increased permeability and, thus, noncardiogenic pulmonary edema. Ventilation-perfusion lung studies have demonstrated that the predominant pathogenesis of hypoxemia in ARDS is related to intrapulmonary shunts. Common symptoms include dyspnea, tachypnea, dry cough, retrosternal discomfort, and moderate to severe respiratory distress. In most cases the diagnosis of ARDS is that of exclusion. The mainstay of therapy for this syndrome is the management of the underlying disorder causing it. To date, there are no specific pharmacologic interventions of proven value for the treatment of ARDS. Once the potentially treatable sources have been found and their therapy started, the main treatment for ARDS is supportive.
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PMID:Adult respiratory distress syndrome (ARDS): the basics. 816 9

Infectious esophagitis may be caused by fungal, viral, bacterial or even parasitic agents. Risk factors include antibiotics and steroids use, chemotherapy and/or radiation therapy, malignancies and immunodeficiency syndromes including acquired immunodeficiency syndrome. Acute onset of symptoms such as dysphagia and odynophagia is typical. It can coexist with heartburn, retrosternal discomfort, nausea and vomiting. Abdominal pain, anorexia, weight loss and even cough are present sometimes. Infectious esophagitis is predominantly caused by Candida species. Other important causes include cytomegalovirus and herpes simplex virus infection.
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PMID:Etiology, diagnosis and treatment of infectious esophagitis. 2486 80